U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Omega-3 Fatty Acids

; ; .

Author Information and Affiliations

Last Update: January 17, 2023.

Continuing Education Activity

Omega-3 fatty acids are a medication used to manage and treat hyperlipidemia, and it is in the antilipemic class of drugs. This activity outlines the indications, actions, and contraindications for omega-3 fatty acids as a valuable agent in managing hyperlipidemia (and other disorders when applicable). This activity will highlight the mechanism of action, adverse event profile, and other key factors (e.g., off-label uses, dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions) pertinent for members of the healthcare team in the management of patients with hyperlipidemia and related conditions.


  • Identify the indications for omega-3 fatty acid administration/use.
  • Explain the mechanisms of action of omega-3 fatty acids.
  • Describe the adverse effects of omega-3 fatty acids.
  • Review the appropriate monitoring when administering omega-3 fatty acids.
Access free multiple choice questions on this topic.


Omega-3 fatty acids (OM3FAs) are unsaturated fatty acids with at least one double bond located between the third and fourth omega end carbon. Currently, the three most clinically relevant omega-3 polyunsaturated fatty acids (PUFAs) are α-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Oils containing these fatty acids originate in plant sources and can be found in fish, fish products, seeds, nuts, green leafy vegetables, and beans.[1][2]

Currently, the FDA has approved the use of two prescription omega-3 fatty acids products, icosapent ethyl and omega-3-acid ethyl esters. Omega-3-carboxylic acids and omega-3-acid ethyl esters A are two prescription omega-3 fatty acids formulations that have since been discontinued. Omega-3-acid ethyl esters,omega-3-carboxylic acids, and omega-3-acid ethyl esters A contain both EPA and DHA, whereas icosapent ethyl contains ethyl esters of EPA only.[3] Iosapent ethyl and omega-3-acid ethyl esters are approved for adults (≥18 years of age) with very high triglycerides (≥ 500 mg/dl) as an adjunct to diet to decrease triglyceride levels and reduce cardiovascular events.[4][5][3][6] These prescription OM3FA products have also been recommended in adjunctive therapy in combination with statins to provide an enhanced reduction of the total cholesterol/high-density lipoprotein cholesterol in comparison to statin alone.[7][8][9] However, some studies have urged physicians to proceed with caution when prescribing a statin/DHA OM3FA combination due to the possibility of increased low-density lipoprotein (LDL) cholesterol.[7][10][11] DHA containing OM3FA can be switched to EPA-only icosapent ethyl that is not associated with increased LDL.[10][11]

 It is important to note that while these prescription OM3FA products are the only FDA approved products for the treatment of hypertriglyceridemia, ongoing research is currently investigating the significance of OM3FAs and their promising role in the treatment of conditions and ailments listed below:

  • Cardiovascular disease[1][12][13][14] 
  • Hypertriglyceridemia (200 to 499 mg/dL)[4]
  • Type 2 diabetes[1]
  • Alzheimer disease and dementia[1] 
  • Depression[1]
  • Visual and neurological/brain development[1]
  • Maternal health during pregnancy and child health[1]
  • Conditions benefiting from prebiotics[17]
  • Heart failure[18][13]
  • Intervertebral disc degeneration[19]
  • Attention deficit hyperactivity disorder[20][21]
  • Maternal depression[22]
  • Menopausal night sweats[23]
  • Rheumatoid arthritis[1][14]
  • Periodontal disease[1][26]
  • Epilepsy[27][28]
  • Diabetic retinopathy[2][29]
  • Efficacy, tolerability, and side-effects of chemotherapy[30][1][31]
  • Premenstrual syndrome[32]
  • Non-alcoholic fatty liver disease[33]

Omega-3 intake and/or supplementation have been shown to be beneficial in treating the above conditions; however, much controversy still exists in many of the above uses. More research with well-conducted clinical trials will need to be completed before definitive conclusions can be made.

Mechanism of Action

The mechanism of action of OM3FAs to lower triglycerides (FDA approved use) is still not fully known but is thought to lower triglycerides by suppressing lipogenic gene expression, increasing beta-oxidation of fatty acids, increasing the expression of lipo-protein-lipase (LPL), and influencing total body lipid accretion.[34][35][36]

OM3FAs suppress lipogenic gene expression by decreasing the expression of sterol regulatory element-binding protein 1c, inhibiting phosphatidic acid phosphatase, and acyl-CoA:1,2-diacylglycerol acyltransferase (NGAT). Sterol regulatory element-binding proteins (SREBP's) are membrane-bound enzymes that, when cleaved, travel to the nucleus to transcribe enzymes involved in cholesterol, LDL, and fatty acid synthesis. When a diet is high in omega-3 fatty acids, the SREBPs (particularly 1c) are not activated because of negative feedback inhibition and lowers SREBP synthesis and the cholesterol synthesizing enzymes that it regulates; FPP synthase (farnesyl diphosphate synthase) and HMG-CoA reductase (3-hydroxy-3-methylglutaryl-CoA reductase).[37][38]

 Beta oxidation is the biological pathway used in the body to break down fat and converts it into energy.[35] OM3FAs decrease the level of triacylglycerides in the body by increasing the rate of beta-oxidation by acting specifically on carnitine acetyltransferase 1 (CAT 1) and acetyl-CoA carboxylase.[34][35] Carnitine acetyltransferase acts to modify fatty acid substrates to enter the inner mitochondrial membrane via the carnitine-acylcarnitine translocation properly. Later, it is converted to acyl-CoA, a precursor substrate to acetyl-CoA used to create ATP in various metabolic pathways.[35] Additionally, EPA also indirectly increases beta-oxidation by slowing feedback inhibition.[35] EPA inhibits acetyl-CoA carboxylase, which is the enzyme that catalyzes the synthesis of malonyl CoA, a strong inhibitor of CAT1.[35] By decreasing the amount of malonyl CoA produced, CAT1 will have increased activity and use more triacylglycerides for beta-oxidation. OM3FAs have also been shown to decrease the sensitivity of CAT1 to malonyl CoA.[35]

Lipoprotein lipase (LPL) is an extracellular enzyme found on the endothelium of vascular tissue that functions to remove triacylglycerol components of chylomicrons, low-density lipoproteins (LDL), and very-low-density lipoproteins (VLDL) in the blood.[39][40][41] A diet high in OM3FAs has been shown to increase the expression of LPL and subsequent lipoprotein lipase protein on the endothelial lining and a decrease in the size of chylomicrons.[42] By increasing the amount of lipoprotein lipase and decreasing LDL, VLDL, and chylomicron size, triglycerides can be lower in hypertriglyceridemia patients.

OM3FAs are also believed to reduce high triglycerides by influencing total body lipid accretion. Several studies have found that prolonged use of OM3FAs for more than six weeks can increase the body's metabolic rate and decrease total body fat.[43][35][44] More specifically, study participants showed an increase in lean muscle mass, decreased fat mass, an increase in resting metabolic rate, increased energy expenditure during exercise, and increased fat oxidation both during rest and exercise.[43][35][45][44] On a cellular level, this is caused by OM3FAs ability to act as a ligand for peroxisome proliferator-activated receptors (PPARs), whose transcription factor activity can change gene expression involved in energy homeostasis.[43][46] PPARs regulate both fatty acid metabolism (beta-oxidation) and glucose metabolism and can change the basal metabolism of the cell.[47] The increase in fat oxidation and energy needs by changes in body composition is thought to be another mechanism by which OM3FAs help lower the triglyceride levels in the blood.

Additional mechanisms of action appear to exist for OM3FAs that explain the beneficial effects on the brain, brain development, cancer, diabetes, rheumatoid arthritis, irritable bowel disease, and the cardiovascular system outside of triglyceride regulation. Most of these effects are attributed to OM3FAs' anti-inflammatory actions. Omega-3 Fatty Acids have been shown to modulate several inflammatory pathways such as[18][48][15][49][50]:

  • Inhibition of leukocyte chemotaxis
  • Inhibitions of adhesion molecule expression (like leukocyte-endothelial adhesive interactions)
  • Inhibition of cyclooxygenase (COX) activity and its subsequent eicosanoid production, like leukotrienes and prostaglandins from arachidonic acid
  • Inhibition of proinflammatory cytokines (e.g., TNF-alpha, IL-1, IL-6)
  • Increase production of inflammation resolving resolvins, maresins, lipoxins, and protectins
  • Inhibition of pro-inflammatory transcription nuclear factor kappa B (nuclear factor-kB) activation
  • Activation of anti-inflammatory transcription factor NR1C3
  • Activation of PPARs
  • Activation of G protein-coupled receptor GPR120
  • Altering phospholipid fatty acid composition
  • Disrupting lipid rafts

Although many cancers are helped by OM3FAs anti-inflammatory effect and non-small-cell lung cancer tumor growth has shown to decrease by inhibiting acetyl-CoA carboxylase (decreasing fatty acid production), other antineoplastic mechanisms of OM3FAs have been shown to be beneficial for other cancers, such as breast cancer, colorectal cancer, leukemia, gastric cancer, pancreatic cancer, esophageal cancer, prostate cancer, head and neck cancer, as well as lung cancer.[51][15] OM3FAs activate AMPK/SIRT, which is involved in cell maintenance and repair, producing an antineoplastic effect that is useful in cancer treatment.[50][15]

OM3FAs have a stabilizing and protecting effect for certain tissues with high-fat content, like neural and retinal tissue.  Alzheimer disease, dementia, and cognitive function are improved by OM3FAs ability to maintain cell membrane integrity of neural tissues because DHA is an essential component of the brain's phospholipid membranes.[52][53][54] Additionally, macular degeneration can be helped with the supplement of DHA for structural support and EPA-based eicosanoids for neovascular and cell survival because DHA and EPA are also integral components of retinal cell membranes.[55]

OM3FAs have some cardioprotective effects that help protect against heart failure in congestive heart failure (CHF) patients. OM3FAs, specifically DHA, decrease mitochondrial oxygen consumption without reducing power generation for the ventricles by altering the mitochondrial membrane phospholipid composition, protecting the heart from tiring.[18]  Whereas EPA inhibits the apoptotic activity stimulated by saturated fatty acid cardiac lipotoxicity, protecting the heart from injury.[18] OM3FAs can protect from arrhythmia by inhibiting inward sodium current in a dose-dependent manner, suppressing intracellular calcium (Ca2+) waves, and helping strengthen autonomic tone.[56] OM3FAs can also vasodilate and decrease blood pressure or afterload to help the heart pump easier because they stimulate nitrous oxide (NO) release from vascular endothelial tissue.[18] OM3FAs also protect the heart through their antithrombotic and antiatherosclerotic abilities.  OM3FAs have been shown to suppress platelet-derived thromboxane A2 (TXA2) synthesis, which constricts blood vessels and aids in platelet aggregation, and reduces the production of matrix metalloproteinases released by macrophages when there is endothelial injury.[18][57]

It should be noted that numerous studies continue to determine the exact mechanisms by which OM3FAs have a pharmacological effect. Many studies with conflicting data continue to challenge our current understanding of how OM3FAs can help other conditions beyond hypertriglyceridemia.



The FDA-approved uses of omega-3 fatty acids for adults (≥18 years of age) with hypertriglyceridemia (≥ 500 mg/dl) as an adjunct to diet and exercise are as follows[3][4][6]:

  • Icosapent ethyl is administered as capsules with a daily dose of 4 g/day taken as two, 2-gram capsules twice a day with meals.
  • Omega-3-acid ethyl esters are administered as capsules with a daily dose of 4 g/day taken as 4 capsules once a day with meals or two capsules twice a day with meals.
  • Omega-3-carboxylic acids are administered as capsules with a daily dose of 2 g/day taken as 2 capsules once per day or 4 g/day taken as 4 capsules once a day. Clinical trial administration was without regard to meals.
  • Omega-3-acid ethyl esters A are administered as capsules with a daily dose of 4 g/day taken as 4 capsules once a day with meals or two capsules twice a day with meals.

All OM3FA supplements should be taken whole without being crushed, chewed, or dissolved in the mouth. If a dose is missed, the patient should take it as soon as they remember and should not take a double dose if it is time for their next capsule. Various dietary supplements in different chemical forms are currently available over the counter but have not been FDA approved; hence they are not required to show safety and efficacy before marketing the product.[3]


Humans do not possess the enzymes required to synthesize OM3FAs; therefore, they are considered essential fatty acids because they must be obtained from the diet. OM3FAs are mainly consumed in our diets as fish and plant sources but can also be consumed via prescription OM3FA products.[58] Alpha-linoleic acid (ALA) is a common OM3FA found in seeds and nuts and can be converted to both DHA and EPA inside the body. However, research has found the conversion of DHA from ALA is particularly low, suggesting the importance of direct dietary intake of DHA.[1][59] OM3FAs may be present in several forms, such as triacylglycerols, free fatty acids (FFA), phospholipids, and ethyl esters.[1] Icosapent ethyl, omega-3-acid ethyl esters, and omega-3-acid ethyl esters A are all in the ethyl ester form, whereas; omega-3-carboxylic acids are in the free fatty acid form.[6]

Digestion of OM3FAs begins in the stomach with gastric lipases that break down triacylglycerols into diacylglycerol and fatty acids.[1] Once broken down, they form fat globules that are subsequently broken down by pancreatic lipases and bile salts in the small intestines. The ethyl esters (icosapent ethyl, omega-3-acid ethyl esters, and omega-3-acid ethyl esters A) are principally broken down by pancreatic carboxylic acid ester lipase in the small intestine to form FFA-EPA and FFA-DHA.[1] Monoacylglycerols and the free fatty acids then passively diffuse into enterocytes as micelles.[1] Fatty acids can also be transported into enterocytes by various fatty acid transport proteins present in the enterocyte membrane.[60] Once within the enterocyte, the fatty acids are then re-esterified into triacylglycerols in the endoplasmic reticulum that then bind to apolipoproteins to form chylomicrons.[1][60] Chylomicrons are subsequently exocytosed into the lymphatic system and ultimately enter circulation at the thoracic duct to reach target tissues.[1][60]

While most metabolism of DHA and EPA takes place via beta-oxidation in the liver (as discussed above), cytochrome P450 (CYP)-mediated metabolism is a minor pathway in the breakdown of DHA and EPA.[61]


In the digestion process, the ethyl esters are principally broken down by pancreatic carboxylic acid ester lipase, an enzyme with activity enhanced by high-fat content meals.[1] Moreover, the fat content of a meal can affect the absorption of ethyl esters.[1] Subsequently, absorption of the ethyl esters and icosapent ethyl (EPA formulation only) is decreased when fasting, so it is recommended they are consumed with food.[4] Regarding the absorption of EPA versus DHA, it is thought that EPA is not absorbed as well as DHA and is metabolized faster; thus, there is a higher ratio of DHA to EPA within the serum plasma.[60]

Since OM3FAs may be present in several forms, such as triacylglycerols, free fatty acids, phospholipids, and ethyl esters, the form in which the OM3FA acid is in will affect bioavailability.[1] The suggested bioavailability based on form (lipid structure) from highest to lowest is as follows: phospholipids, re-esterified triacylglycerols, triacylglycerols, free fatty acids, ethyl esters.[58] However, the order is based on lipid structure only and does not reflect other factors that affect the bioavailability OM3FAs, such as the fat content of a meal.[58]

In addition to the form of the OM3FA, the chemical positioning may also affect bioavailability. Some research suggests OM3FA is greater in fish oil due to the OM3FA typically being in the sn-2 position versus marine mammal oils with the OM3FAs in the sn-1 and sn-3 positions.[58][1] Conversely, other sources state that OM3FAs bioavailability is increased in the sn-1 and sn-3 position due to increased accessibility for lipase hydrolysis, so controversy remains regarding how the position affects the bioavailability of the OM3FAs.[58][60] Bioavailability also varies depending on the dietary source. For example, krill oil is known to have high bioavailability compared to other marine sources.[58][60]

Bioavailability of EPA only and both EPA/DHA formulations did not differ based on age or ethnicity; however, the combination formulation bioavailability differed based on gender. Women seem to have higher EPA serum levels than males in the mixed EPA/DHA formulations. However, research on the availability of EPA and DHA of over-the-counter supplements has indicated that age can play a factor in their levels within the plasma.[60] It has also been found that serum EPA increases in a dose-dependent manner when administered with ethyl esters, but serum DHA does not.[6]


Not all of the half-lives of the prescription OM3FA products have been established. The maximum amount of plasma EPA and DHA can be determined within five to nine hours post-administration.[58] However, persistent EPA and DHA serum levels will not be apparent until two weeks of daily supplementation.[58] With repeated administration, the half-life of EPA is 37 hours and 48 hours for DHA.[58]

Adverse Effects

The FDA-approved fatty acid prescriptions (icosapent ethyl, omega-3-acid ethyl esters,omega-3-carboxylic acids, and omega-3-acid ethyl esters A) are generally safe with benign side effects such as fishy taste, eructation, dyspepsia, diarrhea, gas, nausea, and arthralgia.[4][62][63] Adverse reactions seen in clinical trials for each of the FDA approved OM3FA products are as follows[4][3][6]:

Icosapent ethyl: arthralgia and oropharyngeal pain.

Omega-3-acid ethyl esters: eructation, dyspepsia, taste perversion, constipation, GI disorder, vomiting, increased ALT/AST, pruritus, rash.

Omega-3-carboxylic acids: Diarrhea, nausea, abdominal pain or discomfort, eructation, abdominal distension, constipation, vomiting, fatigue, nasopharyngitis, arthralgia, dysgeusia.

Omega-3-acid ethyl esters A: Eructation, dyspepsia, taste perversion, constipation, GI disorder, vomiting, increased ALT/AST, pruritus, rash.


Caution and periodic monitoring are recommended in patients taking antiplatelet and anticoagulant medication due to the ability of omega-3 fatty acids to reduce platelet activity.[4][15] Additionally, omega-3 fatty acids are not considered allergenic, but the FDA labels state to use with caution in patients allergic to seafood. The OM3FAs products are contraindicated for those who have hypersensitivity to the individual formulation.[4]

EPA and DHA can act as alternative substrates for CYP450 metabolism and are partially metabolized by the CYP450 metabolic pathway, however significant inhibition of CYP450 enzymes by DHA or EPA has not been observed and no drug-drug interactions have been established with medications that use the CYP450 metabolic pathway. EPA exclusive supplements have shown to have no drug-drug interactions with other medications that may use the P450 metabolic pathway, such as omeprazole, warfarin, atorvastatin, and rosiglitazone. DHA has shown to have no interactions with other statin drugs.


It is recommended that the healthcare provider monitor the direct low-density lipoprotein (LDL) cholesterol for patients taking the DHA-containing products omega-3-acid ethyl esters, omega-3-acid ethyl esters A, and omega-3-carboxylic acids due to DHA’s association with an increase in LDL cholesterol.[6]

In patients with dyslipidemia, icosapent ethyl is an option since it has no association with increased LDL cholesterol.[3][4][6] For patients with hepatic impairment, monitoring of the AST and ALT should also be done.[6] In patients with paroxysmal or persistent atrial fibrillation, the prescription products containing omega-3-acid ethyl esters and omega-3-acid ethyl esters A have a possible association with increased recurrences of symptomatic atrial fibrillation or flutter.[6]


EPA and DHA are considered generally safe. The FDA recommends that daily intake not exceed 3 g/day of EPA and DHA combined, with no more than 2 g/day deriving from supplements.

Caution is necessary when taking high doses as it may reduce immune function because of changes in the inflammatory response and may cause bleeding problems. EPA and DHA have not been found to be carcinogenic or mutagenic in human models, but icosapent ethyl (EPA only formulation) has shown benign neoplasm growth in murine models.

The FDA-approved fatty acid prescriptions (icosapent ethyl, omega-3-acid ethyl esters,omega-3-carboxylic acids, and omega-3-acid ethyl esters A) are all pregnancy category C drugs, and it is unknown if the drug can cause fetal harm or can affect reproductive capacity. Conversely, some studies concluded that pregnant mothers should incorporate DHA into their diet via high DHA content food or supplements to increase latency and birth weight.[64] 

Additionally, it is not recommended that nursing mothers take DHA or EPA supplements because they can be highly concentrated (possibly 6 to 14 times serum levels), requiring only 200 to 300 mg DHA intake per day in a nursing mother.[65]

Methyl mercury, a toxic organometallic cation, is found in fish. Individuals who use fish as their primary source of OM3FAs or pregnant and nursing women should limit their intake to two to four servings of fish a week and/or replace fish that are high in methyl mercury, such as swordfish, albacore tuna, dolphinfish, kingfish, and shark and replace with fish that have a lower amount of methylmercury, such as salmon, herring, sardines, and trout.[66][67][68] Fortunately, DHA and EPA supplements do not contain methylmercury.

Enhancing Healthcare Team Outcomes

Proper patient education on dosage and use of the prescription EPA-only icosapent ethyl and DHA/EPA formulations are necessary to ensure that the patient achieves the therapeutic benefits. The responsibility of the interprofessional healthcare team, including physicians, nurse practitioners, pharmacists, etc. is to ensure the patient is aware of the possible adverse effects, especially for individuals on polypharmacy with multiple comorbidities, like those with hepatic and pancreatic impairment, those taking anticoagulants, and individuals with a possible fish sensitivity. Proper physician education on considerations when prescribing, monitoring, and stopping treatment is also necessary.

Current FDA guidelines approve DHA and EPA for use in patients with very high triglycerides in conjunction with proper diet and exercise. The patient should be encouraged to eat a balanced diet (low in cholesterol) and regular exercise. Routine monitoring should occur when prescribing icosapent ethyl (EPA only) and DHA/EPA formulation to patients with hypertriglyceridemia to check the level of triglycerides and AST and ALT for hepatic function. Care is also necessary when prescribing EPA and DHA to pregnant and nursing patients because of unknown toxicity to the fetus and infant. Additionally, pharmacists and physicians should inform the patient that better absorption of EPA and DHA occurs when co-administered with food. 

The healthcare team should remain knowledgeable of other potential indications for DHA and EPA use. It is also available over the counter, and patients may take it even if it is not recommended. Physicians and pharmacists could help patients taking over-the-counter EPA and DHA supplements by informing them of foods that they could incorporate into their diet if they wanted to stop using the supplements. Furthermore, physicians should inquire about patients' diets to ensure proper DHA and EPA levels are achieved and fish high in methyl mercury are avoided.

Review Questions


Shahidi F, Ambigaipalan P. Omega-3 Polyunsaturated Fatty Acids and Their Health Benefits. Annu Rev Food Sci Technol. 2018 Mar 25;9:345-381. [PubMed: 29350557]
Behl T, Kotwani A. Omega-3 fatty acids in prevention of diabetic retinopathy. J Pharm Pharmacol. 2017 Aug;69(8):946-954. [PubMed: 28481011]
Fialkow J. Omega-3 Fatty Acid Formulations in Cardiovascular Disease: Dietary Supplements are Not Substitutes for Prescription Products. Am J Cardiovasc Drugs. 2016 Aug;16(4):229-239. [PMC free article: PMC4947114] [PubMed: 27138439]
Skulas-Ray AC, Wilson PWF, Harris WS, Brinton EA, Kris-Etherton PM, Richter CK, Jacobson TA, Engler MB, Miller M, Robinson JG, Blum CB, Rodriguez-Leyva D, de Ferranti SD, Welty FK., American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Lifestyle and Cardiometabolic Health; Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Omega-3 Fatty Acids for the Management of Hypertriglyceridemia: A Science Advisory From the American Heart Association. Circulation. 2019 Sep 17;140(12):e673-e691. [PubMed: 31422671]
Li R, Jia Z, Zhu H. Dietary Supplementation with Anti-Inflammatory Omega-3 Fatty Acids for Cardiovascular Protection: Help or Hoax? React Oxyg Species (Apex). 2019 Mar;7(20):78-85. [PMC free article: PMC6407714] [PubMed: 30854465]
Ito MK. A Comparative Overview of Prescription Omega-3 Fatty Acid Products. P T. 2015 Dec;40(12):826-57. [PMC free article: PMC4671468] [PubMed: 26681905]
Choi HD, Chae SM. Comparison of efficacy and safety of combination therapy with statins and omega-3 fatty acids versus statin monotherapy in patients with dyslipidemia: A systematic review and meta-analysis. Medicine (Baltimore). 2018 Dec;97(50):e13593. [PMC free article: PMC6320142] [PubMed: 30558030]
Kim CH, Han KA, Yu J, Lee SH, Jeon HK, Kim SH, Kim SY, Han KH, Won K, Kim DB, Lee KJ, Min K, Byun DW, Lim SW, Ahn CW, Kim S, Hong YJ, Sung J, Hur SH, Hong SJ, Lim HS, Park IB, Kim IJ, Lee H, Kim HS. Efficacy and Safety of Adding Omega-3 Fatty Acids in Statin-treated Patients with Residual Hypertriglyceridemia: ROMANTIC (Rosuvastatin-OMAcor iN residual hyperTrIglyCeridemia), a Randomized, Double-blind, and Placebo-controlled Trial. Clin Ther. 2018 Jan;40(1):83-94. [PubMed: 29223557]
Barter P, Ginsberg HN. Effectiveness of combined statin plus omega-3 fatty acid therapy for mixed dyslipidemia. Am J Cardiol. 2008 Oct 15;102(8):1040-5. [PMC free article: PMC2915759] [PubMed: 18929706]
Gutstein AS, Copple T. Cardiovascular disease and omega-3s: Prescription products and fish oil dietary supplements are not the same. J Am Assoc Nurse Pract. 2017 Dec;29(12):791-801. [PubMed: 29280361]
Weintraub HS. Overview of prescription omega-3 fatty acid products for hypertriglyceridemia. Postgrad Med. 2014 Nov;126(7):7-18. [PubMed: 25387209]
Calder PC, Deckelbaum RJ. Editorial: Omega-3 fatty acids and cardiovascular outcomes: an update. Curr Opin Clin Nutr Metab Care. 2019 Mar;22(2):97-102. [PubMed: 30585800]
Endo J, Arita M. Cardioprotective mechanism of omega-3 polyunsaturated fatty acids. J Cardiol. 2016 Jan;67(1):22-7. [PubMed: 26359712]
Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002 Oct;56(8):365-79. [PubMed: 12442909]
Nabavi SF, Bilotto S, Russo GL, Orhan IE, Habtemariam S, Daglia M, Devi KP, Loizzo MR, Tundis R, Nabavi SM. Omega-3 polyunsaturated fatty acids and cancer: lessons learned from clinical trials. Cancer Metastasis Rev. 2015 Sep;34(3):359-80. [PubMed: 26227583]
Jing K, Wu T, Lim K. Omega-3 polyunsaturated fatty acids and cancer. Anticancer Agents Med Chem. 2013 Oct;13(8):1162-77. [PubMed: 23919748]
Costantini L, Molinari R, Farinon B, Merendino N. Impact of Omega-3 Fatty Acids on the Gut Microbiota. Int J Mol Sci. 2017 Dec 07;18(12) [PMC free article: PMC5751248] [PubMed: 29215589]
Sakamoto A, Saotome M, Iguchi K, Maekawa Y. Marine-Derived Omega-3 Polyunsaturated Fatty Acids and Heart Failure: Current Understanding for Basic to Clinical Relevance. Int J Mol Sci. 2019 Aug 18;20(16) [PMC free article: PMC6719114] [PubMed: 31426560]
NaPier Z, Kanim LEA, Arabi Y, Salehi K, Sears B, Perry M, Kim S, Sheyn D, Bae HW, Glaeser JD. Omega-3 Fatty Acid Supplementation Reduces Intervertebral Disc Degeneration. Med Sci Monit. 2019 Dec 14;25:9531-9537. [PMC free article: PMC6929565] [PubMed: 31836696]
Chang JP, Su KP, Mondelli V, Pariante CM. Omega-3 Polyunsaturated Fatty Acids in Youths with Attention Deficit Hyperactivity Disorder: a Systematic Review and Meta-Analysis of Clinical Trials and Biological Studies. Neuropsychopharmacology. 2018 Feb;43(3):534-545. [PMC free article: PMC5669464] [PubMed: 28741625]
Bozzatello P, Brignolo E, De Grandi E, Bellino S. Supplementation with Omega-3 Fatty Acids in Psychiatric Disorders: A Review of Literature Data. J Clin Med. 2016 Jul 27;5(8) [PMC free article: PMC4999787] [PubMed: 27472373]
Hsu MC, Tung CY, Chen HE. Omega-3 polyunsaturated fatty acid supplementation in prevention and treatment of maternal depression: Putative mechanism and recommendation. J Affect Disord. 2018 Oct 01;238:47-61. [PubMed: 29860183]
Mohammady M, Janani L, Jahanfar S, Mousavi MS. Effect of omega-3 supplements on vasomotor symptoms in menopausal women: A systematic review and meta-analysis. Eur J Obstet Gynecol Reprod Biol. 2018 Sep;228:295-302. [PubMed: 30056356]
Brigham EP, Woo H, McCormack M, Rice J, Koehler K, Vulcain T, Wu T, Koch A, Sharma S, Kolahdooz F, Bose S, Hanson C, Romero K, Diette G, Hansel NN. Omega-3 and Omega-6 Intake Modifies Asthma Severity and Response to Indoor Air Pollution in Children. Am J Respir Crit Care Med. 2019 Jun 15;199(12):1478-1486. [PMC free article: PMC6580674] [PubMed: 30922077]
Kumar A, Mastana SS, Lindley MR. n-3 Fatty acids and asthma. Nutr Res Rev. 2016 Jun;29(1):1-16. [PubMed: 26809946]
Chee B, Park B, Fitzsimmons T, Coates AM, Bartold PM. Omega-3 fatty acids as an adjunct for periodontal therapy-a review. Clin Oral Investig. 2016 Jun;20(5):879-94. [PubMed: 26885664]
Bahagat KA, Elhady M, Aziz AA, Youness ER, Zakzok E. [Omega-6/omega-3 ratio and cognition in children with epilepsy]. An Pediatr (Engl Ed). 2019 Aug;91(2):88-95. [PubMed: 30660389]
Tejada S, Martorell M, Capó X, Tur JA, Pons A, Sureda A. Omega-3 Fatty Acids in the Management of Epilepsy. Curr Top Med Chem. 2016;16(17):1897-905. [PubMed: 26845549]
Rosenberg K. Omega-3 Fatty Acid Intake Lowers Risk of Diabetic Retinopathy. Am J Nurs. 2017 Jan;117(1):60-61. [PubMed: 28030412]
de la Rosa Oliva F, Meneses García A, Ruiz Calzada H, Astudillo de la Vega H, Bargalló Rocha E, Lara-Medina F, Alvarado Miranda A, Matus-Santos J, Flores-Díaz D, Oñate-Acuña LF, Gutiérrez-Salmeán G, Ruiz García E, Ibarra A. Effects of omega-3 fatty acids supplementation on neoadjuvant chemotherapy-induced toxicity in patients with locally advanced breast cancer: a randomized, controlled, double-blinded clinical trial. Nutr Hosp. 2019 Aug 26;36(4):769-776. [PubMed: 31192682]
Bahmanyar S, Higgins GA, Goldgaber D, Lewis DA, Morrison JH, Wilson MC, Shankar SK, Gajdusek DC. Localization of amyloid beta protein messenger RNA in brains from patients with Alzheimer's disease. Science. 1987 Jul 03;237(4810):77-80. [PubMed: 3299701]
Behboudi-Gandevani S, Hariri FZ, Moghaddam-Banaem L. The effect of omega 3 fatty acid supplementation on premenstrual syndrome and health-related quality of life: a randomized clinical trial. J Psychosom Obstet Gynaecol. 2018 Dec;39(4):266-272. [PubMed: 28707491]
Spooner MH, Jump DB. Omega-3 fatty acids and nonalcoholic fatty liver disease in adults and children: where do we stand? Curr Opin Clin Nutr Metab Care. 2019 Mar;22(2):103-110. [PMC free article: PMC6355343] [PubMed: 30601174]
Backes J, Anzalone D, Hilleman D, Catini J. The clinical relevance of omega-3 fatty acids in the management of hypertriglyceridemia. Lipids Health Dis. 2016 Jul 22;15(1):118. [PMC free article: PMC4957330] [PubMed: 27444154]
Noreen EE, Sass MJ, Crowe ML, Pabon VA, Brandauer J, Averill LK. Effects of supplemental fish oil on resting metabolic rate, body composition, and salivary cortisol in healthy adults. J Int Soc Sports Nutr. 2010 Oct 08;7:31. [PMC free article: PMC2958879] [PubMed: 20932294]
Bays HE, Tighe AP, Sadovsky R, Davidson MH. Prescription omega-3 fatty acids and their lipid effects: physiologic mechanisms of action and clinical implications. Expert Rev Cardiovasc Ther. 2008 Mar;6(3):391-409. [PubMed: 18327998]
Le Jossic-Corcos C, Gonthier C, Zaghini I, Logette E, Shechter I, Bournot P. Hepatic farnesyl diphosphate synthase expression is suppressed by polyunsaturated fatty acids. Biochem J. 2005 Feb 01;385(Pt 3):787-94. [PMC free article: PMC1134755] [PubMed: 15473864]
Horton JD, Bashmakov Y, Shimomura I, Shimano H. Regulation of sterol regulatory element binding proteins in livers of fasted and refed mice. Proc Natl Acad Sci U S A. 1998 May 26;95(11):5987-92. [PMC free article: PMC27572] [PubMed: 9600904]
Pirahanchi Y, Anoruo M, Sharma S. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 30, 2023. Biochemistry, Lipoprotein Lipase. [PubMed: 30725725]
He PP, Jiang T, OuYang XP, Liang YQ, Zou JQ, Wang Y, Shen QQ, Liao L, Zheng XL. Lipoprotein lipase: Biosynthesis, regulatory factors, and its role in atherosclerosis and other diseases. Clin Chim Acta. 2018 May;480:126-137. [PubMed: 29453968]
Mead JR, Irvine SA, Ramji DP. Lipoprotein lipase: structure, function, regulation, and role in disease. J Mol Med (Berl). 2002 Dec;80(12):753-69. [PubMed: 12483461]
Park Y, Harris WS. Omega-3 fatty acid supplementation accelerates chylomicron triglyceride clearance. J Lipid Res. 2003 Mar;44(3):455-63. [PubMed: 12562865]
Logan SL, Spriet LL. Omega-3 Fatty Acid Supplementation for 12 Weeks Increases Resting and Exercise Metabolic Rate in Healthy Community-Dwelling Older Females. PLoS One. 2015;10(12):e0144828. [PMC free article: PMC4682991] [PubMed: 26679702]
Couet C, Delarue J, Ritz P, Antoine JM, Lamisse F. Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults. Int J Obes Relat Metab Disord. 1997 Aug;21(8):637-43. [PubMed: 15481762]
Kopecky J, Rossmeisl M, Flachs P, Kuda O, Brauner P, Jilkova Z, Stankova B, Tvrzicka E, Bryhn M. n-3 PUFA: bioavailability and modulation of adipose tissue function. Proc Nutr Soc. 2009 Nov;68(4):361-9. [PubMed: 19698199]
Seo T, Blaner WS, Deckelbaum RJ. Omega-3 fatty acids: molecular approaches to optimal biological outcomes. Curr Opin Lipidol. 2005 Feb;16(1):11-8. [PubMed: 15650558]
Kota BP, Huang TH, Roufogalis BD. An overview on biological mechanisms of PPARs. Pharmacol Res. 2005 Feb;51(2):85-94. [PubMed: 15629253]
Calder PC. Omega-3 fatty acids and inflammatory processes: from molecules to man. Biochem Soc Trans. 2017 Oct 15;45(5):1105-1115. [PubMed: 28900017]
Calder PC. Omega-3 polyunsaturated fatty acids and inflammatory processes: nutrition or pharmacology? Br J Clin Pharmacol. 2013 Mar;75(3):645-62. [PMC free article: PMC3575932] [PubMed: 22765297]
Ishihara T, Yoshida M, Arita M. Omega-3 fatty acid-derived mediators that control inflammation and tissue homeostasis. Int Immunol. 2019 Aug 23;31(9):559-567. [PubMed: 30772915]
Svensson RU, Parker SJ, Eichner LJ, Kolar MJ, Wallace M, Brun SN, Lombardo PS, Van Nostrand JL, Hutchins A, Vera L, Gerken L, Greenwood J, Bhat S, Harriman G, Westlin WF, Harwood HJ, Saghatelian A, Kapeller R, Metallo CM, Shaw RJ. Inhibition of acetyl-CoA carboxylase suppresses fatty acid synthesis and tumor growth of non-small-cell lung cancer in preclinical models. Nat Med. 2016 Oct;22(10):1108-1119. [PMC free article: PMC5053891] [PubMed: 27643638]
Chew EY, Clemons TE, Agrón E, Launer LJ, Grodstein F, Bernstein PS., Age-Related Eye Disease Study 2 (AREDS2) Research Group. Effect of Omega-3 Fatty Acids, Lutein/Zeaxanthin, or Other Nutrient Supplementation on Cognitive Function: The AREDS2 Randomized Clinical Trial. JAMA. 2015 Aug 25;314(8):791-801. [PMC free article: PMC5369607] [PubMed: 26305649]
Sydenham E, Dangour AD, Lim WS. Omega 3 fatty acid for the prevention of cognitive decline and dementia. Cochrane Database Syst Rev. 2012 Jun 13;(6):CD005379. [PubMed: 22696350]
Tully AM, Roche HM, Doyle R, Fallon C, Bruce I, Lawlor B, Coakley D, Gibney MJ. Low serum cholesteryl ester-docosahexaenoic acid levels in Alzheimer's disease: a case-control study. Br J Nutr. 2003 Apr;89(4):483-9. [PubMed: 12654166]
SanGiovanni JP, Chew EY. The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina. Prog Retin Eye Res. 2005 Jan;24(1):87-138. [PubMed: 15555528]
Nodari S, Metra M, Milesi G, Manerba A, Cesana BM, Gheorghiade M, Dei Cas L. The role of n-3 PUFAs in preventing the arrhythmic risk in patients with idiopathic dilated cardiomyopathy. Cardiovasc Drugs Ther. 2009 Feb;23(1):5-15. [PubMed: 18982439]
Haglund O, Mehta JL, Saldeen T. Effects of fish oil on some parameters of fibrinolysis and lipoprotein(a) in healthy subjects. Am J Cardiol. 1994 Jul 15;74(2):189-92. [PubMed: 8023790]
Cholewski M, Tomczykowa M, Tomczyk M. A Comprehensive Review of Chemistry, Sources and Bioavailability of Omega-3 Fatty Acids. Nutrients. 2018 Nov 04;10(11) [PMC free article: PMC6267444] [PubMed: 30400360]
Anderson BM, Ma DW. Are all n-3 polyunsaturated fatty acids created equal? Lipids Health Dis. 2009 Aug 10;8:33. [PMC free article: PMC3224740] [PubMed: 19664246]
Schuchardt JP, Hahn A. Bioavailability of long-chain omega-3 fatty acids. Prostaglandins Leukot Essent Fatty Acids. 2013 Jul;89(1):1-8. [PubMed: 23676322]
Arnold C, Konkel A, Fischer R, Schunck WH. Cytochrome P450-dependent metabolism of omega-6 and omega-3 long-chain polyunsaturated fatty acids. Pharmacol Rep. 2010 May-Jun;62(3):536-47. [PubMed: 20631419]
Brinton EA, Mason RP. Prescription omega-3 fatty acid products containing highly purified eicosapentaenoic acid (EPA). Lipids Health Dis. 2017 Jan 31;16(1):23. [PMC free article: PMC5282870] [PubMed: 28137294]
Fabian CJ, Kimler BF, Hursting SD. Omega-3 fatty acids for breast cancer prevention and survivorship. Breast Cancer Res. 2015 May 04;17(1):62. [PMC free article: PMC4418048] [PubMed: 25936773]
Saccone G, Berghella V. Omega-3 long chain polyunsaturated fatty acids to prevent preterm birth: a systematic review and meta-analysis. Obstet Gynecol. 2015 Mar;125(3):663-672. [PubMed: 25730231]
Section on Breastfeeding. Breastfeeding and the use of human milk. Pediatrics. 2012 Mar;129(3):e827-41. [PubMed: 22371471]
Zamora-Arellano NY, Betancourt-Lozano M, Ilizaliturri-Hernández C, García-Hernández J, Jara-Marini M, Chávez-Sánchez C, Ruelas-Inzunza JR. Mercury Levels and Risk Implications Through Fish Consumption on the Sinaloa Coasts (Gulf of California, Northwest Mexico). Risk Anal. 2018 Dec;38(12):2646-2658. [PubMed: 30229961]
García-Hernández J, Ortega-Vélez MI, Contreras-Paniagua AD, Aguilera-Márquez D, Leyva-García G, Torre J. Mercury concentrations in seafood and the associated risk in women with high fish consumption from coastal villages of Sonora, Mexico. Food Chem Toxicol. 2018 Oct;120:367-377. [PubMed: 30026089]
Mozaffarian D, Rimm EB. Fish intake, contaminants, and human health: evaluating the risks and the benefits. JAMA. 2006 Oct 18;296(15):1885-99. [PubMed: 17047219]

Disclosure: Kristina Krupa declares no relevant financial relationships with ineligible companies.

Disclosure: Kristina Fritz declares no relevant financial relationships with ineligible companies.

Disclosure: Mayur Parmar declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK564314PMID: 33231984


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

  • Rivastigmine.[StatPearls. 2024]
    Patel PH, Gupta V. StatPearls. 2024 Jan
  • Benazepril.[StatPearls. 2024]
    Dahal SS, Gupta M. StatPearls. 2024 Jan
  • Etoposide.[StatPearls. 2024]
    Reyhanoglu G, Tadi P. StatPearls. 2024 Jan
  • Triamterene.[StatPearls. 2024]
    Niyazov R, Sharman T. StatPearls. 2024 Jan
  • Muscarinic Antagonists.[StatPearls. 2024]
    Muscarinic Antagonists.
    Naji A, Gatling JW. StatPearls. 2024 Jan
See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...